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RPS12

S. cerevisiae

40S ribosomal protein eS12 RPS12

What the model saw

Gene: RPS12
Organism: Saccharomyces cerevisiae
Known functions: 40S ribosomal protein eS12 RPS12. structural constituent of ribosome.
View unredacted entry
40S ribosomal protein eS12 RPS12. structural constituent of ribosome.

Solver output

Predicted influence
Anti-longevity
Confidence
72%
Mechanism
Deregulated nutrient sensing
Reasoning

RPS12 encodes the 40S ribosomal small subunit protein eS12, a structural constituent of the ribosome. Ribosome biogenesis and translational capacity are tightly coupled to the TOR (Target of Rapamycin) nutrient-sensing pathway in yeast; elevated ribosomal activity downstream of TORC1 promotes growth but accelerates aging. Reduction of ribosomal protein gene dosage — including deletion of individual RP genes such as RPS12 — is well-established in S. cerevisiae to extend both replicative and chronological lifespan, consistent with the idea that normal ribosomal function drives pro-growth, pro-aging signaling. The mechanism likely involves reduced translational output dampening TORC1-driven anabolic programs and potentially activating autophagy/proteostasis pathways. Thus, the normal (wild-type) function of RPS12 — supporting ribosome assembly and translation — opposes longevity.

Key pathways
TOR/TORC1 nutrient-sensing and ribosome biogenesis40S ribosomal small subunit assemblytranslational regulation of aging
Longevity influence
Anti-longevity
Lifespan effect
Increase

GenAge curators classify each gene's normal function as promoting (Pro-Longevity) or opposing (Anti-Longevity) longevity, based on synthesis across studies. Loss-of-function effects can vary from this depending on the manipulation.

Advisor judgment

Answer
Correct
Mechanism
Correct
Reasoning quality
5/5
Failure mode
Correct
Notes

The model correctly predicted anti_longevity for RPS12 in S. cerevisiae. The mechanistic reasoning is sound and well-articulated: ribosomal protein genes are well-established anti-longevity factors in yeast, as deletion of RP genes (including RPS12) extends lifespan by reducing translational output and dampening TORC1-driven anabolic programs. The connection to TOR/nutrient-sensing pathway is appropriate and well-supported by the literature. The model correctly identifies that wild-type RPS12 function (supporting ribosome assembly and translation) opposes longevity. Confidence of 0.72 is reasonable given the general knowledge about RP gene deletions extending lifespan in yeast.

Raw API responses

solver

{
  "reasoning": "RPS12 encodes the 40S ribosomal small subunit protein eS12, a structural constituent of the ribosome. Ribosome biogenesis and translational capacity are tightly coupled to the TOR (Target of Rapamycin) nutrient-sensing pathway in yeast; elevated ribosomal activity downstream of TORC1 promotes growth but accelerates aging. Reduction of ribosomal protein gene dosage — including deletion of individual RP genes such as RPS12 — is well-established in S. cerevisiae to extend both replicative and chronological lifespan, consistent with the idea that normal ribosomal function drives pro-growth, pro-aging signaling. The mechanism likely involves reduced translational output dampening TORC1-driven anabolic programs and potentially activating autophagy/proteostasis pathways. Thus, the normal (wild-type) function of RPS12 — supporting ribosome assembly and translation — opposes longevity.",
  "confidence": 0.72,
  "key_pathways": [
    "TOR/TORC1 nutrient-sensing and ribosome biogenesis",
    "40S ribosomal small subunit assembly",
    "translational regulation of aging"
  ],
  "mechanism_class": "deregulated_nutrient_sensing",
  "longevity_influence": "anti_longevity"
}

advisor

{
  "notes": "The model correctly predicted anti_longevity for RPS12 in S. cerevisiae. The mechanistic reasoning is sound and well-articulated: ribosomal protein genes are well-established anti-longevity factors in yeast, as deletion of RP genes (including RPS12) extends lifespan by reducing translational output and dampening TORC1-driven anabolic programs. The connection to TOR/nutrient-sensing pathway is appropriate and well-supported by the literature. The model correctly identifies that wild-type RPS12 function (supporting ribosome assembly and translation) opposes longevity. Confidence of 0.72 is reasonable given the general knowledge about RP gene deletions extending lifespan in yeast.",
  "failure_mode": "correct",
  "answer_correct": true,
  "mechanism_correct": true,
  "reasoning_quality": 5,
  "ground_truth_questionable": false
}